JUNG-TSU CHENCHEN-YING WANGMIN-HUEY CHEN2021-07-202021-07-202018-120929-6646https://scholars.lib.ntu.edu.tw/handle/123456789/572080Many fibrotic processes are associated with an increased level of transforming growth factor-β1 (TGF-β1). TGF-β1 can increase synthesis of matrix proteins and enhance secretion of protease inhibitors, resulting in matrix accumulation. Connective tissue growth factor (CTGF) is a downstream profibrotic effector of TGF-β1 and is associated with the fibrosis in several human organs. Curcumin has been applied to reduce matrix accumulation in fibrotic diseases. This study was aimed to evaluate whether curcumin could suppress TGF-β1-induced CTGF expression and its related signaling pathway involving in this inhibitory action in primary human gingival fibroblasts.enConnective tissue growth factor; Curcumin; Gingival overgrowth; Smad2; Transforming growth factor-β1[SDGs]SDG3connective tissue growth factor; curcumin; phenytoin; Smad2 protein; transforming growth factor beta receptor 1; transforming growth factor beta1; connective tissue growth factor; curcumin; Smad2 protein; transforming growth factor beta1; Article; cell viability; controlled study; endothelium cell; epithelium cell; fibroblast; gingiva overgrowth; gingival biopsy; gingival tissue; human; human cell; human tissue; immunoblotting; immunohistochemistry; inflammatory cell; MTT assay; protein expression; signal transduction; smooth muscle cell; antagonists and inhibitors; cell culture; chemically induced; drug effect; fibroblast; gingiva overgrowth; metabolism; phosphorylation; Cells, Cultured; Connective Tissue Growth Factor; Curcumin; Epithelial Cells; Fibroblasts; Gingival Overgrowth; Humans; Phosphorylation; Signal Transduction; Smad2 Protein; Transforming Growth Factor beta1journal article10.1016/j.jfma.2017.12.014293390382-s2.0-85044718490https://scholars.lib.ntu.edu.tw/handle/123456789/416427